Despite its enormous impact on public health, we have only a limited understanding of the molecular mechanisms underlying influenza A virus (IAV) ability to evade the immune response. Antigenic drift precludes long lasting natural or vaccine induced immunity, and is the cause of yearly vaccine reformulation. Despite its importance, we have only a limited understanding of the molecular mechanisms underlying antigenic drift of IAV and the fine specificity of the B cell response to the IAV hemagglutinin. We are examining the changes in the structure and function of the influenza HA that provide an advantage in the face of the host neutralizing antibody response. This year we have been examining the role of non-infectious/semi-infectious virions during virus infection. Our studies suggest that the traditional propagation dependent assays of infectivity underestimate the true infectious potential of a virus population.